Cadherins the primary regulators of the overall state of epithelial cell contact and facilitate an appropriate cytoskeletal organization and the establishment of many other kinds of cell interactions that preserve tissue integrity, thereby leading to the establishment of the density dependent inhibition of growth. However, it remains obscure whether E-cadherin directly transfers growth inhibitory signals to the cells, or if other types of molecular cell interactions indirectly influenced by the establishment of cadherin mediated cell contacts, are responsible for contact inhibition of growth. In this study I selectively activate the formation of E-cadherin homophilic adhesive bonds, using a specific recombinant protein to engage E-cadherin molecules at the cell surface of dispersed primary breast epithelial cells. Here I show evidence that E-cadherin ligation is capable to reduce the rate of cells entered into S-phase, in a process not linked with apoptosis. beta-catenin/TCF signaling activity does not appear to be involved in the inhibition of cell growth, since the cells did not displayed constitutive beta-catenin/TCF signaling. Moreover, direct inhibition of beta-catenin/TCF signaling pathway was not able to decrease the proliferation rate in these cells, suggesting the involvement of other growth inhibitory signaling pathways in this event.

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